NFKB1 and serum lipopolysaccharide activity: Disruption of epithelial tight junctions increases endotoxin translocation (circulating Lipopolysaccharide (LPS)), activates hepatic Toll-like receptor 4 (TLR4) and Nuclear Factor-kappa B (NF-κB) signaling, and worsens insulin resistance; conversely, fermented-food matrices and their derivatives recurrently tighten the barrier and lower endotoxemia in preclinical models, with concordant improvements in liver inflammation and metabolism [145,146].